Effect of prednisolone on myocardial infarct healing: characteristics and comparison with indomethacin.

MedLine Citation:

PMID:
1768984
Owner:
NLM
Status:
MEDLINE

Abstract/OtherAbstract:

OBJECTIVE: To characterize retardation of myocardial infarct healing by corticosteroid administration, and to examine the role of suppression of prostaglandin production in its effect. DESIGN: The left circumflex coronary artery of the rabbit was occluded for 30 mins and reperfused for 72 h. Rabbits were divided into four groups: a control group, a low dose prednisolone group (L-PSL) that was treated with 5 mg/kg/24 h prednisolone, a high dose prednisolone group (H-PSL) that was treated with 10 mg/kg/24 h prednisolone, and an indomethacin group that received a 5 mg/kg intravenous bolus of indomethacin followed by 10 mg/kg/24 h. The status of infarct healing and infarcted wall thinning was assessed 72 h after ischemia by the percentage of infarct mass organized (%O/I) and the ratio of infarcted wall thickness to noninfarcted wall thickness (thinning ratio). MAIN RESULTS: The %O/I was 61.4 +/- 4.2% (mean +/- SEM) in the control group. The L-PSL and H-PSL groups had %O/Is of 48.3 +/- 3.7% and 29.1 +/- 2.1%, respectively, which were significantly lower than the control value. The difference in %O/I between the H-PSL and L-PSL groups was also significant. However, the %O/I of the indomethacin group (55.1 +/- 3.3%) was not significantly different from control. When the myocardial infarcts were retrospectively subgrouped into small infarcts (infarct volume less than 0.31 cm3) and large infarcts (greater than or equal to 0.31 cm3), infarct healing delay in large infarcts was evident only for H-PSL and not for L-PSL, while both L-PSL and H-PSL treatment retarded healing of small infarcts. No significant difference was observed in the thinning ratio for any group. CONCLUSION: Infarct healing delay by prednisolone is dosage dependent, and smaller infarcts may be more sensitive to its effect. Retardation of infarct healing by prednisolone is unlikely to be mediated by suppression of prostaglandins from the cyclo-oxygenase pathway.